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<title>Journal of Parenteral and Enteral Nutrition</title>
<url>http://pen.sagepub.com:80/icons/banner/title.gif</url>
<link>http://pen.sagepub.com</link>
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<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/6/588?rss=1">
<title><![CDATA[A.S.P.E.N. Clinical Guidelines: Nutrition Support of Children With Human Immunodeficiency Virus Infection]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/6/588?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Sabery, N., Duggan, C., the American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) Board of Directors]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109346276</dc:identifier>
<dc:title><![CDATA[A.S.P.E.N. Clinical Guidelines: Nutrition Support of Children With Human Immunodeficiency Virus Infection]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>606</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>588</prism:startingPage>
<prism:section>Clinical Guidelines</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/607?rss=1">
<title><![CDATA[Butyrate Increases GLUT2 mRNA Abundance by Initiating Transcription in Caco2-BBe Cells]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/607?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Glucose transporter 2 (GLUT2) is a high-capacity,
facilitative intestinal monosaccharide transporter, known to be upregulated by
short-chain fatty acids (SCFAs) derived from the intestinal microbiota during
fermentation. Understanding the mechanisms regulating intestinal function is
important to optimize therapies for patients with intestinal failure and
ultimately reduce their dependence on parenteral nutrition.
<I>Objective:</I> The objective was to examine the mechanism regulating the
underlying response of GLUT2 to the SCFA butyrate. <I>Methods:</I> GLUT2
messenger RNA (mRNA) abundance was measured in differentiated Caco2-BBe
monolayers treated for 0.5-24 hours with 0-20 mM butyrate using quantitative
reverse transcription&ndash;polymerase chain reaction. Activation of the human
GLUT2 promoter was measured using luciferase reporting in transiently
transfected Caco2-BBe monolayers. <I>Results:</I> GLUT2 mRNA abundance was
higher (<I>P</I> &lt; .0001) with 1-4 hours of exposure to 2.5, 7.5, and 10
mM butyrate. Butyrate induced (<I>P</I> &lt; .0001) promoter activity in a
dose-dependent fashion. Analysis of the GLUT2 promoter indicated that regions
&ndash;282/+522, &ndash;216/+522, and &ndash;145/+522 had a heightened
(<I>P</I> &lt; .05) response to butyrate compared with 1135/+522 and
564/+522. <I>Conclusions:</I> Butyrate upregulates GLUT2 mRNA abundance in
Caco2-BBe monolayers by activating specific regions within the human GLUT2
promoter. These results identify a cellular mechanism wherein butyrate
upregulates intestinal absorption that may be relevant to patients with
reduced function. Additional work is necessary to understand cellular targets
of butyrate therapy and define clinically appropriate means of providing such
strategies, such as consuming prebiotics and probiotics.</p>
]]></description>
<dc:creator><![CDATA[Mangian, H. F., Tappenden, K. A.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336599</dc:identifier>
<dc:title><![CDATA[Butyrate Increases GLUT2 mRNA Abundance by Initiating Transcription in Caco2-BBe Cells]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>617</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>607</prism:startingPage>
<prism:section>2009 Harry M. Vars Research Award</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/618?rss=1">
<title><![CDATA[Enteral Refeeding Rapidly Restores PN-Induced Reduction of Hepatic Mononuclear Cell Number Through Recovery of Small Intestine and Portal Vein Blood Flows]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/618?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Absence of enteral nutrition (EN) reduces hepatic
mononuclear cell (MNC) numbers and impairs their functions. However, enteral
refeeding (ER) for as little as 12 hours following parenteral nutrition (PN)
rapidly restores hepatic MNC numbers. We hypothesized that changes in small
intestine and portal vein blood flows related to feeding route might be
responsible for this phenomenon. <I>Methods:</I> In experiment 1, mice (n =
19) were randomized to Chow (n = 5), PN (n = 7) or ER (n = 7) groups. The Chow
group was given chow <I>ad libitum</I> with intravenous (IV) saline for 5
days. The PN group was fed parenterally for 5 days, while the ER group was
re-fed with chow for 12 hours following 5 days of PN. Then, small intestine
and portal vein blood flows were monitored and hepatic MNCs were isolated and
counted. In experiment 2, the effects of intravenous administration of
prostaglandin E<SUB>1</SUB> (PGE<SUB>1</SUB>) on hepatic MNC numbers were
examined in fasted mice for 12 hours. Mice (n = 28) were randomized to Control
(n = 8), PG0 (n = 10), or PG1 (n = 10) groups. The Control group was fed chow
<I>ad libitum</I> with IV saline, while the PG0 and PG1 groups were fasted
for 12 hours with infusions, respectively, of saline and PGE<SUB>1</SUB> at 1
&micro;g/kg/minute. Blood flows and hepatic MNC numbers were examined.
<I>Results:</I> Experiment 1: ER restored PN-induced reductions in small
intestine and portal vein blood flows and hepatic MNC number to the levels in
the Chow group. Small intestine and portal vein blood flows correlated
positively with hepatic MNC number. Experiment 2: Fasting decreased small
intestine and portal vein blood flows and hepatic MNC number. However,
PGE<SUB>1</SUB> restored portal vein blood flow to the level of the Control
group, and moderately increased hepatic MNC number. There was a positive
correlation between portal blood flow and hepatic MNC number.
<I>Conclusions:</I> Reduced small intestine and portal vein blood flows may
contribute to impaired hepatic immunity in the absence of EN. ER quickly
restores hepatic MNC number through recovery of blood flow in both the small
intestine and the portal vein.</p>
]]></description>
<dc:creator><![CDATA[Omata, J., Fukatsu, K., Murakoshi, S., Noguchi, M., Miyazaki, H., Moriya, T., Okamoto, K., Fukazawa, S., Akase, T., Saitoh, D., Mochizuki, H., Yamamoto, J., Hase, K.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336598</dc:identifier>
<dc:title><![CDATA[Enteral Refeeding Rapidly Restores PN-Induced Reduction of Hepatic Mononuclear Cell Number Through Recovery of Small Intestine and Portal Vein Blood Flows]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>626</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>618</prism:startingPage>
<prism:section>Premier Research Papers</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/629?rss=1">
<title><![CDATA[Colonic GLP-2 is not Sufficient to Promote Jejunal Adaptation in a PN-Dependent Rat Model of Human Short Bowel Syndrome]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/629?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Bowel resection may lead to short bowel syndrome
(SBS), which often requires parenteral nutrition (PN) due to inadequate
intestinal adaptation. The objective of this study was to determine the time
course of adaptation and proglucagon system responses after bowel resection in
a PN-dependent rat model of SBS. <I>Methods:</I> Rats underwent jugular
catheter placement and a 60% jejunoileal resection + cecectomy with
jejunoileal anastomosis or transection control surgery. Rats were maintained
exclusively with PN and killed at 4 hours to 12 days. A nonsurgical group
served as baseline. Bowel growth and digestive capacity were assessed by
mucosal mass, protein, DNA, histology, and sucrase activity. Plasma
insulin-like growth factor I (IGF-I) and bioactive glucagon-like peptide 2
(GLP-2) were measured by radioimmunoassay. <I>Results:</I> Jejunum
cellularity changed significantly over time with resection but not
transection, peaking at days 3-4 and declining by day 12. Jejunum
sucrase-specific activity decreased significantly with time after resection
and transection. Colon crypt depth increased over time with resection but not
transection, peaking at days 7-12. Plasma bioactive GLP-2 and colon
proglucagon levels peaked from days 4-7 after resection and then approached
baseline. Plasma IGF-I increased with resection through day 12. Jejunum and
colon GLP-2 receptor RNAs peaked by day 1 and then declined below baseline.
<I>Conclusions:</I> After bowel resection resulting in SBS in the rat, peak
proglucagon, plasma GLP-2, and GLP-2 receptor levels are insufficient to
promote jejunal adaptation. The colon adapts with resection, expresses
proglucagon, and should be preserved when possible in massive intestinal
resection.</p>
]]></description>
<dc:creator><![CDATA[Koopmann, M. C., Liu, X., Boehler, C. J., Murali, S. G., Holst, J. J., Ney, D. M.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336597</dc:identifier>
<dc:title><![CDATA[Colonic GLP-2 is not Sufficient to Promote Jejunal Adaptation in a PN-Dependent Rat Model of Human Short Bowel Syndrome]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>639</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>629</prism:startingPage>
<prism:section>Premier Research Papers</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/640?rss=1">
<title><![CDATA[Measurement of Resting Energy Expenditure in Healthy Children]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/640?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> The role that the components of energy expenditure
play in the etiology of childhood obesity has highlighted the need for greater
accuracy and standardized protocols for the measurement of resting energy
expenditure (REE). However, protocols used to assess REE in children are
varied, and consensus on a suitable method for measuring REE in children has
not been reached. This study was undertaken to determine the effect of
measurement time and measurement device (mask or mouthpiece) on REE in healthy
children. <I>Design:</I> Following a 12-hour fast and abstinence from
exercise, 23 children (age, 7&ndash;12 years) completed two 35-minute
protocols: one with a face mask and the other with a mouthpiece/noseclip.
Energy expenditure was measured continuously via indirect calorimetry, while
device acceptability was assessed using a 6-point comfort rating scale.
<I>Results:</I> Repeated measures ANOVA indicated that there was no
significant difference in REE when measured after 10, 15, 20, or 25 minutes of
rest compared to 30 minutes for either the mask or mouthpiece/noseclip (REE
range, 1371&ndash;1460 kcal/d). Examination of the percentage coefficient of
varia tion (CV) in energy expenditure for each time period by device showed
that the least variation existed after 20 minutes of measurement using the
mask (CV 6%). Paired <I>t</I> test analysis indicated significantly less
discomfort when wearing the mask compared to the mouthpiece/noseclip.
<I>Conclusion:</I> It would appear that a 20-minute protocol using a mask
may increase compliance and prove to be a more practical protocol for
measuring REE in children.</p>
]]></description>
<dc:creator><![CDATA[Mellecker, R. R., McManus, A. M.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336603</dc:identifier>
<dc:title><![CDATA[Measurement of Resting Energy Expenditure in Healthy Children]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>645</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>640</prism:startingPage>
<prism:section>Techniques, Materials, and Devices</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/646?rss=1">
<title><![CDATA[Disparate Response to Metoclopramide Therapy for Gastric Feeding Intolerance in Trauma Patients With and Without Traumatic Brain Injury]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/646?rss=1</link>
<description><![CDATA[
<p>Patients with traumatic brain injury (TBI) have delayed gastric emptying
and often require prokinetic drug therapy to improve enteral feeding
tolerance. The authors hypothesized that metoclopramide was less efficacious
for improving gastric feeding tolerance for trauma patients with TBI compared
to trauma patients without TBI. A retrospective analysis was conducted of
patients admitted to the trauma or neurosurgical intensive care unit who
received gastric feeding from January 2006 to April 2008. Gastric feeding
intolerance was defined by a gastric residual volume &gt;200 mL or emesis with
abdominal distension or discomfort. Patients with gastric feeding intolerance
were given metoclopramide 10 mg intravenously every 6 hours, followed by a
dose escalation to 20 mg, and then combination therapy with metoclopramide and
erythromycin 250 mg intravenously every 6 hours if intolerance persisted. In
total, 882 trauma patients (49% with TBI) were evaluated. TBI patients had a
higher incidence of gastric feeding intolerance than those without TBI (18.6%
vs 10.4%, <I>P</I> &le; .001). Efficacy rates for metoclopramide 10 mg,
metoclopramide 20 mg, and metoclopramide-erythromycin were 55%, 62%, and 79%,
respectively (<I>P</I> &le; .03). Metoclopramide failure occurred in 54% of
patients with TBI compared to 35% of patients without TBI, respectively
(<I>P</I> &le; .02), due to a greater prevalence of tachyphylaxis.
Single-drug therapy with metoclopramide was less effective for TBI trauma
patients compared to trauma patients without TBI. Combination therapy with
erythromycin as first-line therapy for TBI trauma patients with gastric
feeding intolerance is indicated if there are no contraindications or
significant drug interactions.</p>
]]></description>
<dc:creator><![CDATA[Dickerson, R. N., Mitchell, J. N., Morgan, L. M., Maish, G. O., Croce, M. A., Minard, G., Brown, R. O.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109335307</dc:identifier>
<dc:title><![CDATA[Disparate Response to Metoclopramide Therapy for Gastric Feeding Intolerance in Trauma Patients With and Without Traumatic Brain Injury]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>655</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>646</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/656?rss=1">
<title><![CDATA[Riboflavin Status in Acutely Ill Patients and Response to Dietary Supplements]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/656?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Although a number of studies have reported riboflavin
deficiency in free-living older people, no data are available on riboflavin
intake and status in older people during acute illness. <I>Methods:</I> To
determine the riboflavin response to dietary supplements during acute illness,
297 hospitalized, acutely ill older patients are randomly assigned to receive
a daily oral nutritional supplement containing 1.3 mg of riboflavin or a
placebo for 6 weeks. Outcome measures are riboflavin intake and riboflavin
biochemical status at baseline, 6 weeks, and 6 months using the erythrocyte
glutathione reductase activation coefficient (EGRAC), a measure of riboflavin
tissue saturation. EGRAC values are inversely proportional to riboflavin
status. <I>Results:</I> Fifty-six percent of patients (167/297) have
suboptimal riboflavin status (EGRAC &gt; 1.30). No significant correlation is
found between EGRAC and either total energy or riboflavin intakes. Significant
correlations are found between total energy intake and riboflavin intakes both
in hospital and at home (<I>r</I> = 0.67, <I>P</I> &lt; .0001 and
<I>r</I> = 0.57, <I>P</I> &lt; .0001, respectively). Smokers and patients
with chronic obstructive pulmonary disease (COPD) have lower riboflavin status
(high EGRAC values) compared with nonsmokers and those without COPD.
Riboflavin status improves significantly in the supplement group at 6 weeks
compared with the placebo group, but status declines between 6 weeks and 6
months, after patients stop taking the supplements. <I>Conclusions:</I> A
high proportion of acutely ill patients have suboptimal riboflavin status.
Supplementation with a physiological amount of riboflavin in a mixed-nutrient
supplement significantly improves riboflavin status, but the effect is
transient and status deteriorates again after patients stop taking the
supplements.</p>
]]></description>
<dc:creator><![CDATA[Gariballa, S., Forster, S., Powers, H.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336602</dc:identifier>
<dc:title><![CDATA[Riboflavin Status in Acutely Ill Patients and Response to Dietary Supplements]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>661</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>656</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/662?rss=1">
<title><![CDATA[Intestinal Redox Status of Major Intracellular Thiols in a Rat Model of Chronic Alcohol Consumption]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/662?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Alcohol consumption is associated with oxidative
stress in multiple tissues in vivo, yet the effect of chronic alcohol intake
on intestinal redox state has received little attention. In this study, we
investigated the redox status of 2 major intracellular redox regulating
couples: glutathione (GSH)/glutathione disulfide (GSSG) and cysteine
(Cys)/cystine (CySS) in a rat model of chronic alcohol ingestion.
<I>Methods:</I> Sprague-Dawley rats were fed the liquid Lieber-DeCarli diet
consisting of 36% ethanol of total calories for 6 weeks. Control rats were
pair-fed with an isocaloric, ethanol-free liquid diet. Defined mucosal samples
from the jejunum, ileum, and colon were obtained and analyzed by
high-performance liquid chromatography (HPLC) for GSH and Cys pool redox
status. Mucosal free malondialdehyde (MDA) was measured as an indicator of
lipid peroxidation. <I>Results:</I> In the ethanol-fed rats, Cys and mixed
disulfide (GSH-Cys) were significantly decreased in all 3 segments of
intestinal mucosa. Free MDA was increased in jejunal but not in ileal or
colonic mucosa. Chronic ethanol ingestion significantly increased mucosal GSH
concentration in association with a more reducing GSH/GSSG redox potential in
the jejunum, but these indices were unchanged in the ileum. In the colon,
chronic ethanol ingestion increased oxidant stress as suggested by decreased
GSH and oxidized GSH/GSSG redox potential. <I>Conclusions:</I> Chronic
alcohol intake differentially alters the mucosal redox status in proximal to
distal intestinal segments in rats. Such changes may reflect different
adaptability of these intestinal segments to the oxidative stress challenge
induced by chronic ethanol ingestion.</p>
]]></description>
<dc:creator><![CDATA[Tian, J., Brown, L. A. S., Jones, D. P., Levin, M. S., Wang, L., Rubin, D. C., Ziegler, T. R.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336600</dc:identifier>
<dc:title><![CDATA[Intestinal Redox Status of Major Intracellular Thiols in a Rat Model of Chronic Alcohol Consumption]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>668</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>662</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/669?rss=1">
<title><![CDATA[Clinical Application of Magnetic Resonance Spectroscopy of the Liver in Patients Receiving Long-Term Parenteral Nutrition]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/669?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Intestinal failure&ndash;associated liver disease
(IFALD) may have progressed to an advanced stage by the time it becomes
evident via laboratory or physical signs. A safe, noninvasive technique for
assessing the liver could significantly aid in monitoring the effects of
therapeutic intervention, improve the timing of liver and small intestinal
transplantation, and increase our understanding of the causes of IFALD.
<I>Methods:</I> Six female patients fed intravenously for &gt;1 year and 6
controls matched for body mass index (BMI) underwent liver magnetic resonance
scanning with acquisition of <sup>1</sup>H and <sup>31</sup>P resonance
spectra. Areas under the curve for lipid (the sum of CH, CH<SUB>2</SUB>, and
CH<SUB>3</SUB>), water, and choline peaks were calculated and expressed
semi-quantitatively as ratios of lipid:water and choline:lipid.
Phosphomonoester (PME) and phosphodiester (PDE) peak areas were similarly
expressed as a ratio. Controls and cases were compared using Mann-Whitney
<I>U</I> test; least squares regression analysis was used to compare the
effect of measured variables on the lipid:water peak area ratio.
<I>Results:</I> Patients and controls were well matched for BMI. Parenteral
feeding was associated with a highly significant increase in lipid:water peak
ratio (<I>P</I> &lt; .005). Choline:lipid (<I>P</I> &lt; .05) and
choline:water (not significant) ratios were reduced in patients compared with
controls. The increase in lipid:water ratios in patients was independent of
BMI and choline:water ratios. A ratio of PME:PDE of &gt;0.3 (and &gt;3 SD from
the control mean) predicted the 2 patients at most risk of advanced liver
disease. <I>Conclusions:</I> This pilot study confirms the potential of
magnetic resonance spectroscopic techniques in evaluating IFALD and could
contribute significantly to our understanding and management of this
condition.</p>
]]></description>
<dc:creator><![CDATA[Woodward, J. M., Priest, A. N., Hollingsworth, K. G., Lomas, D. J.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109332908</dc:identifier>
<dc:title><![CDATA[Clinical Application of Magnetic Resonance Spectroscopy of the Liver in Patients Receiving Long-Term Parenteral Nutrition]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>676</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>669</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/677?rss=1">
<title><![CDATA[Intravascular Embolization of Venous Catheter--Causes, Clinical Signs, and Management: A Systematic Review]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/677?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Intravascular embolization of device fragments is a
rare but potentially serious complication. <I>Method:</I> A systematic
search of the PubMed and MEDLINE databases for all articles pertaining to
central catheter related embolization published in English between 1985 and
2007 was made. <I>Results:</I> A total of 215 cases of intravenous catheter
embolization were identified. There were 143 totally implanted venous devices
(TIVD) or port catheters and 72 percutaneous venous catheters (PVC). Sites of
catheter fragments following embolization were the superior vena cava or
peripheral veins (15.4%), the right atrium (27.6%), right ventricle (22%), and
pulmonary arteries (35%). Clinical signs of catheter embolization included
catheter malfunction (56.3%), arrhythmia (13%), pulmonary symptoms (4.7%), and
septic syndromes (1.8%), but 24.2% of cases were asymptomatic. The causes of
intravascular catheter embolization were pinch-off syndrome (40.9%), catheter
injury during explantation (17.7%), catheter disconnection (10.7%), and
catheter rupture (11.6%). In 19.1% of cases, the cause of catheter
embolization could not be identified. Most embolized catheter fragments
(93.5%) were removed percutaneously. In 4.2% of cases, fragments were retained
in the vascular bed; in 2.3%, embolized fragments were removed surgically via
thoracotomy. <I>Conclusion:</I> Intravascular catheter embolization can go
undiagnosed for prolonged periods. Patients might be asymptomatic or may
develop severe systemic clinical signs. The mortality rate is 1.8%. There were
no significant differences in clinical features of embolization between TIVD
and PVC groups.</p>
]]></description>
<dc:creator><![CDATA[Surov, A., Wienke, A., Carter, J. M., Stoevesandt, D., Behrmann, C., Spielmann, R.-P., Werdan, K., Buerke, M.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109335121</dc:identifier>
<dc:title><![CDATA[Intravascular Embolization of Venous Catheter--Causes, Clinical Signs, and Management: A Systematic Review]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>685</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>677</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/686?rss=1">
<title><![CDATA[Laparoscopic Surgery Improves Blood Glucose Homeostasis and Insulin Resistance Following Distal Gastrectomy for Cancer]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/686?rss=1</link>
<description><![CDATA[
<p><I>Background</I>: Prevention of blood glucose elevation and insulin
resistance could be more pronounced in patients undergoing laparoscopic rather
than open gastrectomy. <I>Methods</I>: Fifty-seven patients underwent distal
gastrectomy by either laparoscopy (n = 36) or an open approach (n = 21). Blood
glucose, serum insulin, and the daily insulin secretion rate (urinary
C-peptide) were measured. Insulin resistance was evaluated using an adapted
homeostasis model assessment of insulin resistance (HOMA-R). <I>Results</I>:
Blood glucose levels were lower in the laparoscopy group than in the open
group on the operative day and on postoperative days (POD) 1 and 3 (<I>P</I>
&lt; .001, <I>P</I> = .001, and <I>P</I> = .024, respectively). Serum
insulin levels were lower in the laparoscopy group than in the open group on
POD 1 and 3 (<I>P</I> = .045 and <I>P</I> = .027, respectively). HOMA-R
was lower in the laparoscopy group than in the open group on POD 1 and 3
(<I>P</I> = .024 and <I>P</I> = .009, respectively). Daily insulin
secretion rates were lower in the laparoscopy group than in the open group on
POD 1 (<I>P</I> = .023). <I>Conclusions</I>: Laparoscopic surgery prevents
blood glucose elevation and improves insulin resistance compared with open
surgery.</p>
]]></description>
<dc:creator><![CDATA[Kanno, H., Kiyama, T., Fujita, I., Tani, A., Kato, S., Tajiri, T., Barbul, A.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109333003</dc:identifier>
<dc:title><![CDATA[Laparoscopic Surgery Improves Blood Glucose Homeostasis and Insulin Resistance Following Distal Gastrectomy for Cancer]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>690</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>686</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/691?rss=1">
<title><![CDATA[Neonatal Parenteral Nutrition Hypersensitivity: A Case Report Implicating Bisulfite Sensitivity in a Newborn Infant]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/691?rss=1</link>
<description><![CDATA[
<p>This report describes a case of parenteral nutrition hypersensitivity in a
37 weeks' gestation infant with congenital diaphragmatic hernia complicated by
bowel necrosis and functional short bowel syndrome. The patient developed a
rash with subsequent urticaria beginning on the 50th day of life. The
reactions were confirmed with a positive rechallenge. After the amino acid
solution was replaced with a non&ndash;bisulfite-containing product, the
infant was able to continue to receive nutrition support through parenteral
nutrition without recurrence of symptoms. It is speculated that the bisulfite
additive in the amino acid solution may have interacted with the lipid
emulsion to sensitize the patient.</p>
]]></description>
<dc:creator><![CDATA[Huston, R. K., Baxter, L. M., Larrabee, P. B.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109347643</dc:identifier>
<dc:title><![CDATA[Neonatal Parenteral Nutrition Hypersensitivity: A Case Report Implicating Bisulfite Sensitivity in a Newborn Infant]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>693</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>691</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/694?rss=1">
<title><![CDATA[Low Availability of Aluminum in Formulations for Parenteral Nutrition Containing Silicate]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/694?rss=1</link>
<description><![CDATA[
<p><I>Background</I>: Silicate (Si) and aluminum (Al) may be concomitant
impurities in solutions for parenteral nutrition (PN). Silicate can bind to Al
to form stable hydroxyaluminosilicates (HAS), thus reducing Al availability.
This possibility is investigated by heating solutions containing constituents
of PN in glass containers to promote the release of Si and Al.
<I>Methods</I>: The total amount of Si and Al in solution is measured by
atomic absorption spectrometry, and the Al not bound to Si is evaluated by
reaction with morin. <I>Results:</I> When the Si:Al molar ratio is &gt;5, no
free Al is found in solution. For ratios &lt;5, it is found that the lower the
ratio, the higher the free Al fraction. However, in solutions of some amino
acids, even with a low Si:Al ratio (&lt;2), the amount of free Al is lower
than that found in other solutions. The same tendency is observed among
commercial formulations. Although in salt solutions the free fraction of Al
reaches almost 100% when the Si concentration is low, in amino acid
formulations the free fraction of Al does not surpass 50%. Moreover, even for
Si:Al ratios &gt;5, there is a "residual" fraction of free Al in
amino acid formulations. <I>Conclusions</I>: The concomitant presence of Al
and Si in solutions for PN reduces the amount of Al available attributable to
the formation of HAS. In amino acid formulations this effect may be slightly
reduced given the affinity of certain amino acids for Al. Therefore, amino
acids may behave in the same fashion as silicate.</p>
]]></description>
<dc:creator><![CDATA[Bohrer, D., Bortoluzzi, F., Nascimento, P. C. d., de Carvalho, L. M., de Oliveira, S. R.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109333004</dc:identifier>
<dc:title><![CDATA[Low Availability of Aluminum in Formulations for Parenteral Nutrition Containing Silicate]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>701</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>694</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/702?rss=1">
<title><![CDATA[Enteral Nutrition and Cardiovascular Failure: From Myths to Clinical Practice]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/702?rss=1</link>
<description><![CDATA[
<p>Cardiovascular failure and low flow states may arise in very different
conditions from both cardiac and noncardiac causes. Systemic hemodynamic
failure inevitably alters splanchnic blood flow but in an unpredictable way.
Prolonged low splanchnic blood flow causes intestinal ischemia, increased
mucosal permeability, endotoxemia, and distant organ failure. Mortality
associated with intestinal ischemia is high. Why would enteral nutrition (EN)
be desirable in these complex patients when parenteral nutrition could easily
cover energy and substrate requirements? Metabolic, immune, and practical
reasons justify the use of EN. In addition, continuous enteral feeding
minimizes systemic and myocardial oxygen consumption in patients with
congestive heart failure. Further, early feeding in critically ill
mechanically ventilated patients has been shown to reduce mortality,
particularly in the sickest patients. In a series of cardiac surgery patients
with compromised hemodynamics, absorption has been maintained, and 1000-1200
kcal/d could be delivered by enteral feeding. Therefore, early EN in
stabilized patients should be attempted, and can be carried out safely under
close clinical monitoring, looking for signs of incipient intestinal ischemia.
Energy delivery and balance should be monitored, and combined feeding
considered when enteral feeds cannot be advanced to target within 4-6
days.</p>
]]></description>
<dc:creator><![CDATA[Berger, M. M., Chiolero, R. L.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109341769</dc:identifier>
<dc:title><![CDATA[Enteral Nutrition and Cardiovascular Failure: From Myths to Clinical Practice]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>709</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>702</prism:startingPage>
<prism:section>CNW 2009 Keynote Address</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/710?rss=1">
<title><![CDATA[Malnutrition Syndromes: A Conundrum vs Continuum]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/710?rss=1</link>
<description><![CDATA[
<p>This provocative commentary critically examines historic definitions for
adult malnutrition syndromes as they apply to developed countries with modern
healthcare. To stimulate further discussion, the authors propose an updated
approach that incorporates current understanding of the systemic inflammatory
response to help guide assessment, diagnosis, and treatment. An appreciation
of a continuum of inflammatory response in relation to malnutrition syndromes
is described. This discussion serves to highlight a research agenda to address
deficiencies in diagnostics, biomarkers, and therapeutics of inflammation in
relation to malnutrition.</p>
]]></description>
<dc:creator><![CDATA[Jensen, G. L., Bistrian, B., Roubenoff, R., Heimburger, D. C.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109344724</dc:identifier>
<dc:title><![CDATA[Malnutrition Syndromes: A Conundrum vs Continuum]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>716</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>710</prism:startingPage>
<prism:section>Invited Commentary</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/717?rss=1">
<title><![CDATA[How Immunocompromised Are Short Bowel Patients Receiving Home Parenteral Nutrition? Apropos a Case of Disseminated Fusarium Oxysporum Sepsis]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/717?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Catheter-related sepsis is the most frequent
complication in patients receiving home parenteral nutrition (HPN) for short
bowel syndrome (SBS). A low-grade systemic inflammatory state and an altered
mucosal immune response, as well as diminished intestinal barrier function
have been characterized in these patients. The possibility of systemic
immunocompromise has only recently been suggested. <I>Case Description:</I>
A 45-year-old female with traumatic SBS was admitted for possible
catheter-related sepsis. She was asplenic and had insulin-dependent diabetes
mellitus as a result of a pancreatic resection. A large skin ulceration was
present on her left calf, which appeared unusual for a disseminated bacterial
infection. Chest x-ray and computed tomography scan revealed multiple
subpleural pulmonary infiltrates consistent with bacterial or fungal
dissemination. Blood cultures from the port system and from the peripheral
blood grew <I>Staphylococcus haemolyticus</I> and <I>Fusarium
oxysporum</I>. The port system was removed, and flucloxacillin and
voriconazole were given for 33 and 35 days, respectively. Clinical signs of
disseminated sepsis resolved slowly. Bone marrow biopsy ruled out primary
hematologic disease. <I>Conclusions:</I> (1) Catheter-related sepsis in
patients on HPN is usually caused by Gram-positive or Gram-negative bacteria
or by <I>Candida</I> species. Identification of molds in blood cultures
strongly suggests <I>Fusarium</I> species, which should be treated
appropriately with voriconazole or amphotericin B. (2) HPN and SBS aggravated
by asplenism and diabetes mellitus can cause severe immunocompromise. (3)
Fusaria have a strong tendency to persist or reappear after bone marrow
transplantation, which is therefore relatively contraindicated in these
patients.</p>
]]></description>
<dc:creator><![CDATA[Muller, C., Schumacher, U., Gregor, M., Lamprecht, G.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109346321</dc:identifier>
<dc:title><![CDATA[How Immunocompromised Are Short Bowel Patients Receiving Home Parenteral Nutrition? Apropos a Case of Disseminated Fusarium Oxysporum Sepsis]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>720</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>717</prism:startingPage>
<prism:section>Case Reports</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/721?rss=1">
<title><![CDATA[Percutaneous Gastrojejunostomy Placement in a Heart Failure Patient With Biventricular Assist Devices]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/721?rss=1</link>
<description><![CDATA[
<p>Heart failure patients who require a ventricular assist device often
present a nutrition challenge. A 39-year-old woman suffering from an acute ST
elevated myocardial infarction and severe cardiogenic shock underwent implant
of left and right ventricular assist devices (BiVAD). Neurologic deficits
prevented her from safely resuming oral intake, and long-term feeding access
was required. The decision was made to insert a percutaneous gastrojejunostomy
under fluoroscopic guidance. Patients implanted with ventricular assist
devices may require enteral nutrition support. Placement of feeding access
other than through the nasoenteric route can be rendered more challenging
because of anatomical constraints related to BiVAD positioning; however,
whenever enteral nutrition support is required for extended periods,
percutaneous or ostomy access offers easier delivery of nutrition. Although
technically difficult, successful placement of the enteral feeding tube
allowed for continuous 24-hour feeds to optimize nutrition intake. This is the
first time that a percutaneous enteral feeding access was obtained for a
ventricular assist device patient at the authors' institution, and it has
proven valuable in providing long-term nutrition in a safe and efficient
manner.</p>
]]></description>
<dc:creator><![CDATA[Page, S., Cecere, R., Valenti, D.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109338214</dc:identifier>
<dc:title><![CDATA[Percutaneous Gastrojejunostomy Placement in a Heart Failure Patient With Biventricular Assist Devices]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>723</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>721</prism:startingPage>
<prism:section>Case Reports</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/6/724?rss=1">
<title><![CDATA[Unanswered Questions of "ProCon"etic Therapy]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/6/724?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[MacLaren, R.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109343591</dc:identifier>
<dc:title><![CDATA[Unanswered Questions of "ProCon"etic Therapy]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>725</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>724</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/6/726?rss=1">
<title><![CDATA[Imaging Biochemistry Noninvasively: Magnetic Resonance Spectroscopy in Liver Disease]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/6/726?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Serkova, N. J.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109344727</dc:identifier>
<dc:title><![CDATA[Imaging Biochemistry Noninvasively: Magnetic Resonance Spectroscopy in Liver Disease]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>728</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>726</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/6/729?rss=1">
<title><![CDATA[Comment on: Measurement of Resting Energy Expenditure in Healthy Children]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/6/729?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> The role that the components of energy expenditure
play in the etiology of childhood obesity has highlighted the need for greater
accuracy and standardized protocols for the measurement of resting energy
expenditure (REE). However, protocols used to assess REE in children are
varied, and consensus on a suitable method for measuring REE in children has
not been reached. This study was undertaken to determine the effect of
measurement time and measurement device (mask or mouthpiece) on REE in healthy
children. <I>Design:</I> Following a 12-hour fast and abstinence from
exercise, 23 children (age, 7&ndash;12 years) completed two 35-minute
protocols: one with a face mask and the other with a mouthpiece/noseclip.
Energy expenditure was measured continuously via indirect calorimetry, while
device acceptability was assessed using a 6-point comfort rating scale.
Results: Repeated measures ANOVA indicated that there was no significant
difference in REE when measured after 10, 15, 20, or 25 minutes of rest
compared to 30 minutes for either the mask or mouthpiece/noseclip (REE range,
1371&ndash;1460 kcal/d). Examination of the percentage coefficient of
variation (CV) in energy expenditure for each time period by device showed
that the least variation existed after 20 minutes of measurement using the
mask (CV 6%). Paired <I>t</I> test analysis indicated significantly less
discomfort when wearing the mask compared to the mouthpiece/noseclip.
<I>Conclusion:</I> It would appear that a 20-minute protocol using a mask
may increase compliance and prove to be a more practical protocol for
measuring REE in children.(<I>JPEN J Parenter Enteral Nutr</I>. 2009;33:640-645)</p>
]]></description>
<dc:creator><![CDATA[Bogucki, E. L.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109343608</dc:identifier>
<dc:title><![CDATA[Comment on: Measurement of Resting Energy Expenditure in Healthy Children]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>730</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>729</prism:startingPage>
<prism:section>eJournal</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/6/731?rss=1">
<title><![CDATA[Prebiotics and Enteral Feeding-Associated Diarrhea]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/6/731?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hegazi, R., Strausbaugh, K., Merritt, R.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109341878</dc:identifier>
<dc:title><![CDATA[Prebiotics and Enteral Feeding-Associated Diarrhea]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>732</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>731</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/6/733?rss=1">
<title><![CDATA[Author Response]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/6/733?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Barrett, J. S, Shepherd, S. J., Gibson, P. R.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109341880</dc:identifier>
<dc:title><![CDATA[Author Response]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>734</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>733</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/6/735?rss=1">
<title><![CDATA[Letter to the Editor]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/6/735?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Williams-Dolan, J. M., Boullata, J. I.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 10:07:44 PST</dc:date>
<dc:identifier>info:doi/10.1177/0148607109345021</dc:identifier>
<dc:title><![CDATA[Letter to the Editor]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>6</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>736</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>735</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/5/470?rss=1">
<title><![CDATA[Can We Make A.S.P.E.N.'s Clinical Nutrition Week the Pre-eminent International Nutrition Meeting?]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/5/470?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[McClave, S. A.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109344687</dc:identifier>
<dc:title><![CDATA[Can We Make A.S.P.E.N.'s Clinical Nutrition Week the Pre-eminent International Nutrition Meeting?]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>471</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>470</prism:startingPage>
<prism:section>On My Mind: An Opportunity to Dialogue with A.S.P.E.N. President Steven A. McClave</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/5/472?rss=1">
<title><![CDATA[A.S.P.E.N. Clinical Guidelines: Nutrition Support Therapy During Adult Anticancer Treatment and in Hematopoietic Cell Transplantation]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/5/472?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[August, D. A., Huhmann, M. B., the American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) Board of Directors]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109341804</dc:identifier>
<dc:title><![CDATA[A.S.P.E.N. Clinical Guidelines: Nutrition Support Therapy During Adult Anticancer Treatment and in Hematopoietic Cell Transplantation]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>500</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>472</prism:startingPage>
<prism:section>A.S.P.E.N. Clinical Guidelines</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/5/501?rss=1">
<title><![CDATA[Evolution of Lipid Profile, Liver Function, and Pattern of Plasma Fatty Acids According to the Type of Lipid Emulsion Administered in Parenteral Nutrition in the Early Postoperative Period After Digestive Surgery]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/5/501?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> The metabolic effects of intravenous lipid emulsions
(ILEs) used in parenteral nutrition (PN) depend on their fatty acid
composition. <I>Methods:</I> Subjects in this prospective and randomized
double-blind study were 28 adult patients post digestive surgery. PN was
started after surgery and lasts for 5 days. Randomly, patients receive 1 of 4
different ILEs: medium-chain triglycerides/long-chain triglycerides (soybean
oil; MCT/LCT), olive/soybean oil (oleic), long-chain triglycerides (soybean
oil; LCT), and structured lipid. On days 0 and 6, serum liver function tests
were analyzed for cholesterol, triglycerides, lipoproteins, and serum fatty
acids. <I>Results:</I> No differences were found in the 4 groups according
to their gender, age, body mass index, diagnosis, baseline white blood cell,
C-reactive protein, glucose levels, and other study parameters. Differential
significant changes were not observed in any of the hepatic function
parameters or plasmatic lipid levels between the groups. A significant
decrease was observed in cis monounsaturated fatty acids (MUFAs) and a
significant increase in -6 polyunsaturated fatty acids (PUFAs) and
-3 PUFA values in LCT and structured groups compared with MCT/LCT and
oleic groups, and a tendency for a decrease in trans fatty acids in the oleic
and structured groups was found. <I>Conclusions:</I> All ILEs administered
were safe and well tolerated. The changes in serum fatty acids reflected the
pattern of fatty acids administered with different ILEs. The group receiving
the olive oil emulsion achieved a fatty acid composition of serum lipids that
could offer major therapeutic or biological advantages.</p>
]]></description>
<dc:creator><![CDATA[Puiggros, C., Sanchez, J., Chacon, P., Sabin, P., Rosello, J., Bou, R., Planas, M.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109333001</dc:identifier>
<dc:title><![CDATA[Evolution of Lipid Profile, Liver Function, and Pattern of Plasma Fatty Acids According to the Type of Lipid Emulsion Administered in Parenteral Nutrition in the Early Postoperative Period After Digestive Surgery]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>512</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>501</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/5/513?rss=1">
<title><![CDATA[Inhibition of Gastroesophageal Reflux by Semi-solid Nutrients in Patients With Percutaneous Endoscopic Gastrostomy]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/5/513?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Aspiration is one of the major complications after
percutaneous endoscopic gastrostomy (PEG). The administration of semi-solid
nutrients by means of gastrostomy tube has recently been reported to be
effective in preventing aspiration pneumonia. The effects of semi-solid
nutrients on gastroesophageal reflux, intragastric distribution, and gastric
emptying were evaluated. <I>Methods:</I> Semi-solid nutrients were prepared
by liquid nutrients mixed with agar at the concentration of 0.5%. The
distribution of the administered radiolabeled liquid and semi-solid nutrients
was monitored by a scintillation camera for 15 post-PEG patients. The
percentage of esophageal reflux, the distribution of the proximal and distal
stomach, and the gastric emptying time were evaluated. <I>Results:</I> The
percentage of gastroesophageal reflux was significantly decreased in
semi-solid nutrients (0.82 &plusmn; 1.27%) compared with liquid nutrients
(3.75 &plusmn; 4.25%), whereas the gastric emptying time was not different.
The distribution of semi-solid nutrients was not different from liquid
nutrients in the early phase, whereas higher retention of liquid nutrients in
the proximal stomach was observed in the late phase. <I>Conclusions:</I>
Gastroesophageal reflux was significantly inhibited by semi-solid nutrients.
One of the mechanisms of the inhibition is considered to be an improvement in
the transition from the proximal to distal stomach in semi-solid
nutrients.</p>
]]></description>
<dc:creator><![CDATA[Nishiwaki, S., Araki, H., Shirakami, Y., Kawaguchi, J., Kawade, N., Iwashita, M., Tagami, A., Hatakeyama, H., Hayashi, T., Maeda, T., Saitoh, K.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108327045</dc:identifier>
<dc:title><![CDATA[Inhibition of Gastroesophageal Reflux by Semi-solid Nutrients in Patients With Percutaneous Endoscopic Gastrostomy]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>519</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>513</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/5/520?rss=1">
<title><![CDATA[Intestinal Dipeptide Absorption Is Preserved During Thermal Injury and Cytokine Treatment]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/5/520?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Intestinal barrier function is impaired during thermal
injury; however, the effects of thermal injury on the absorption of dietary
peptides are not well characterized. The purpose of this study was to
determine the impact of thermal injury on dipeptide absorption in rats and to
describe the influence of inflammatory cytokines on the expression of the
oligopeptide transporter PEPT1 and dipeptide permeability in cultured
intestinal cells (Caco-2 cells). <I>Methods:</I> Sprague Dawley rats were
assigned to 30% body surface area burn (n = 7) or sham (n = 8) groups.
Twenty-four hours following burn/sham, the proximal jejunum was cannulated.
The jejunal segment was perfused with buffer containing the dipeptide
glycylsarcosine (Gly-Sar), and intestinal permeability
(<I>P<SUB>eff</SUB></I>) was calculated. For in vitro experiments, Caco-2
cells were grown on permeable supports and treated with tumor necrosis factor
(TNF)-, interleukin (IL)-6, and IL-10 (10 ng/mL) alone and in
combination for 48 hours. The effective apical-to-basolateral permeabilities
(<I>P<SUB>eff</SUB></I>) of Gly-Sar were measured, and PEPT1 expression was
determined using reverse transcription-polymerase chain reaction.
<I>Results:</I> Gly-Sar <I>P<SUB>eff</SUB></I> was similar in burn and
sham rats (6.67 &plusmn; 2.27 <FONT FACE="arial,helvetica">x</FONT> 10<sup>-5</sup> vs 7.58 &plusmn; 2.20
<FONT FACE="arial,helvetica">x</FONT> 10<sup>-5</sup> cm/s, respectively, <I>P</I> = .45). In Caco-2
cells, cytokine treatment did not alter PEPT1 expression (<I>P</I> = .954)
or the <I>P<SUB>eff</SUB></I> of Gly-Sar (<I>P</I> = .806).
<I>Conclusions</I>: Intestinal absorption of the dipeptide Gly-Sar is
preserved 24 hours following thermal injury in rats. Likewise, PEPT1
expression and peptide absorption are preserved following treatment with
TNF-, IL-6, and IL-10 in Caco-2 monolayers. These findings imply that
intestinal dipeptide absorption may be preserved during burn injury. This may
lead to new strategies to optimize enteral protein delivery in burn
patients.</p>
]]></description>
<dc:creator><![CDATA[Foster, D. R., Gonzales, J. P., Amidon, G. L., Welage, L. S.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109333002</dc:identifier>
<dc:title><![CDATA[Intestinal Dipeptide Absorption Is Preserved During Thermal Injury and Cytokine Treatment]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>528</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>520</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/5/529?rss=1">
<title><![CDATA[Feeding Jejunostomy for the Treatment of Severe Hyperemesis Gravidarum: A Case Series]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/5/529?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Hyperemesis gravidarum is severe nausea and vomiting
during pregnancy leading to dehydration, nutrition deficiency, and fetal
morbidity and mortality. Treatment must maintain fluid and electrolyte balance
and caloric intake. Parenteral nutrition is often attempted; however,
complication rates are high. Nutrition via nasoenteric and percutaneous
endoscopic gastrostomy tubes is limited by poor patient tolerance, tube
dislodgement, and altered anatomy in pregnancy. <I>Methods:</I> Women with
hyperemesis gravidarum who failed standard therapy were offered jejunostomy.
All patients underwent surgical jejunostomy in the second trimester. Isotonic
tube feeds were administered to a goal caloric factor calculated by the
Harris-Benedict equation with a correction added for pregnancy. Patients were
monitored until delivery. <I>Results:</I> Five women underwent jejunostomy
placement at our institution between 1998 and 2005. One patient underwent
jejunostomy placement twice for consecutive pregnancies. The mean body weight
loss from prepregnancy was 7.9% (range, 4.0%&ndash;15.9%). Patients underwent
jejunostomy placement between 12 and 26 weeks of gestation (median 14 weeks).
Twelve to 16 Fr catheters were placed in the proximal jejunum. Maternal weight
gain occured in 5 of 6 pregnancies. The mean duration of tube placement was 19
weeks (range, 8&ndash;28 weeks). All pregnancies ended with term deliveries
(range, 36&ndash;40 weeks of gestation). The mean infant birth weight was 2885
g (range, 2270&ndash;4000 g). Tube-related complications were limited to
dislodgement in 2 patients in the third trimester. No cases of infection,
bleeding, or preterm labor occured. <I>Conclusions:</I> Feeding via
jejunostomy is a potentially safe, effective, and well-tolerated mode of
nutrition support therapy in hyperemesis gravidarum.</p>
]]></description>
<dc:creator><![CDATA[Saha, S., Loranger, D., Pricolo, V., Degli-Esposti, S.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109333000</dc:identifier>
<dc:title><![CDATA[Feeding Jejunostomy for the Treatment of Severe Hyperemesis Gravidarum: A Case Series]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>534</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>529</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/5/535?rss=1">
<title><![CDATA[Parenteral Feeding Depletes Pulmonary Lymphocyte Populations]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/5/535?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> The effect of parenteral nutrition (PN) on lymphocyte
mass in the lung is unknown, but reduced mucosal lymphocytes are hypothesized
to play a role in the reduced immunoglobulin A&ndash;mediated immunity in both
gut and lung. The ability to transfer and track cells between mice may allow
study of diet-induced mucosal immune function. The objectives of this study
are to characterize lung T-cell populations following parenteral feeding and
to study distribution patterns of transferred donor lung T cells in recipient
mice. <I>Methods:</I> In experiment 1, cannulated male Balb/c mice are
randomized to receive chow or PN for 5 days. Lung lymphocytes are obtained via
collagenase digestion, and flow cytometric analysis is used to identify total
T (CD3+) and B (CD45/B220+) cells. In experiment 2, isolated lung T cells from
chow-fed male Balb/c mice are pooled and labeled in vitro with a fluorescent
dye (carboxyfluorescein diacetate succinimidyl ester [CFSE]), and 1.1 <FONT FACE="arial,helvetica">x</FONT>
10<sup>8</sup> CFSE+ cells (3.1 <FONT FACE="arial,helvetica">x</FONT> 10<sup>6</sup> T cells) are
transferred to chow-fed Balb/c recipients. Cells recovered from recipient
lungs and intestinal lamina propria (LP) are analyzed by flow cytometry to
determine CFSE/CD3+ T cells at 1, 2, and 7 days. In experiment 3, cells are
transferred to PN-fed recipients. <I>Results:</I> In experiment 1, PN
significantly decreases lung T- and B-cell populations compared with chow
feeding. In experiment 2, CFSE+ T-cell retention is highest on day 1 in lung
and LP, and decreases on day 2. Cells are gone by day 7; 98.1% of retained
donor lung T cells migrate to recipient lungs and 1.9% to the intestine on day
1. Similar results are seen in experiment 3 after transfer of cells to PN-fed
recipients. <I>Conclusions:</I> PN reduces pulmonary lymphocyte populations
consistent with impaired respiratory immunity. Transferred lung T cells
preferentially localize to recipient lungs rather than intestine with maximal
accumulation at 24 hours. Limited cross-talk of transferred lung T cells to
the intestine indicates that mucosal lymphocyte traffic might be programmed to
localize to specific effector sites.</p>
]]></description>
<dc:creator><![CDATA[Hermsen, J. L., Gomez, F. E., Sano, Y., Kang, W., Maeshima, Y., Kudsk, K. A.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109332909</dc:identifier>
<dc:title><![CDATA[Parenteral Feeding Depletes Pulmonary Lymphocyte Populations]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>540</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>535</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/5/541?rss=1">
<title><![CDATA[Fish Oil-Based Lipid Emulsions Prevent and Reverse Parenteral Nutrition-Associated Liver Disease: The Boston Experience]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/5/541?rss=1</link>
<description><![CDATA[
<p>Parenteral nutrition&ndash;associated liver disease (PNALD) is the most
prevalent and most severe complication of long-term parenteral nutrition. Its
underlying pathophysiology, however, largely remains to be elucidated. The
currently approved parenteral lipid emulsions in the United States contain
safflower or soybean oils, both rich in -6 polyunsaturated fatty acids
(PUFAs). Mounting evidence indicates that the -6 PUFAs originating from
plant oils in these lipid emulsions may play a role in the onset of liver
injury. Fish oil&ndash;based lipid emulsions, in contrast, are primarily
composed of -3 PUFAs, thus providing a promising alternative. The
authors review the literature on the role of lipid emulsions in the onset of
PNALD and discuss prevention and treatment strategies using a fish
oil&ndash;based lipid emulsion. They conclude that a fish oil&ndash;based
emulsion is hepatoprotective in a murine model of PNALD, and it appears to be
safe and efficacious for the treatment of this type of liver disease in
children. A prospective randomized trial that is currently under way at the
authors' institution will objectively determine the place of fish oil
monotherapy in the prevention of PNALD.</p>
]]></description>
<dc:creator><![CDATA[de Meijer, V. E., Gura, K. M., Le, H. D., Meisel, J. A., Puder, M.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109332773</dc:identifier>
<dc:title><![CDATA[Fish Oil-Based Lipid Emulsions Prevent and Reverse Parenteral Nutrition-Associated Liver Disease: The Boston Experience]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>547</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>541</prism:startingPage>
<prism:section>Reviews</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/5/548?rss=1">
<title><![CDATA[Micronutrient Supplementation in Adult Nutrition Therapy: Practical Considerations]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/5/548?rss=1</link>
<description><![CDATA[
<p>Preexisting micronutrient (vitamins and trace elements) deficiencies are
often present in hospitalized patients. Deficiencies occur due to inadequate
or inappropriate administration, increased or altered requirements, and
increased losses, affecting various biochemical processes and resulting in
organ dysfunction, poor wound healing, and altered immune status with
deleterious sequelae. Guidelines for the 13 essential vitamins and 10
essential trace elements have been established. These recommendations,
however, are applicable to healthy adults and not to critically ill patients,
in whom decreased serum levels may indicate actual deficiencies or a
deficiency due to redistribution. Benefits of supplementation over and above
the daily requirements, which may not result in increased serum levels, are
also unclear and may, in fact, be detrimental. Vitamin requirements are
increased in disease states, but a similar recommendation for trace elements
has not been initiated except for selenium (Se) and zinc (Zn). In practice, a
multivitamin preparation and a multiple trace element admixture (containing
Zn, Se, copper, chromium, and manganese) are added to parenteral nutrition
formulations. Most enteral nutrition preparations also contain adequate
amounts of vitamins and trace elements, although bioavailability may be an
issue. Detailed information about individual micronutrient use specifically in
hospitalized adult patients receiving nutrition therapy will be discussed,
emphasizing the practical and clinical aspects. Clinicians are encouraged to
think of micronutrients not as nutritional supplements alone but also as
therapeutic agents and nutraceuticals.</p>
]]></description>
<dc:creator><![CDATA[Sriram, K., Lonchyna, V. A.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108328470</dc:identifier>
<dc:title><![CDATA[Micronutrient Supplementation in Adult Nutrition Therapy: Practical Considerations]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>562</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>548</prism:startingPage>
<prism:section>Reviews</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/5/563?rss=1">
<title><![CDATA[Racial and Geographic Disparities in the Use of Parenteral Nutrition Among Inflammatory Bowel Disease Inpatients Diagnosed With Malnutrition in the United States]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/5/563?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Racial disparities have been described in the use of a
diverse spectrum of surgical procedures. The objectives of this study are to
determine whether disparities also exist for the use of parenteral nutrition
(PN) in inflammatory bowel disease (IBD). <I>Methods:</I> The U.S.
Nationwide Inpatient Sample between 1998 and 2003 is analyzed to determine PN
use among IBD inpatients diagnosed with protein-calorie malnutrition and
assess whether use patterns differ by race and geographical region.
<I>Results:</I> The proportion of African American IBD admissions with
protein-calorie malnutrition who receive PN is significantly lower than that
in whites (19.9% vs 28.1%, <I>P</I> = .001), whereas there is no difference
between Hispanics and non-Hispanic whites. After adjustment for gender,
comorbidity, health insurance status, geographic region, and median
neighborhood income, African Americans remain less likely than whites to
receive PN (odds ratio [OR] 0.67; 95% confidence interval [CI],
0.50&ndash;0.89), whereas the difference between Hispanics and non-Hispanic
whites is marginally significant (OR 0.65; 95% CI, 0.41&ndash;1.04). PN use
varies geographically, with highest rates in the Northeast (44.3%) and lowest
in the Midwest (17.3%). Uninsured patients are less than half as likely to
receive PN as those with insurance (OR 0.46; 95% CI, 0.31&ndash;0.69).
Compared with whites, Hispanics experience a longer time interval between
admission and initiation of PN (3.5 vs 4.8 days, <I>P</I> = .02) and have
higher rates of catheter-related complications (5.1% vs 12.2%, <I>P</I> =
.04). <I>Conclusions:</I> Among IBD inpatients with clinically diagnosable
malnutrition, PN use is lower among African Americans compared with whites.
The underlying mechanisms of these racial variations merit further
investigation.</p>
]]></description>
<dc:creator><![CDATA[Nguyen, G. C., Munsell, M., Brant, S. R., LaVeist, T. A.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109332907</dc:identifier>
<dc:title><![CDATA[Racial and Geographic Disparities in the Use of Parenteral Nutrition Among Inflammatory Bowel Disease Inpatients Diagnosed With Malnutrition in the United States]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>568</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>563</prism:startingPage>
<prism:section>Brief Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/5/569?rss=1">
<title><![CDATA[Use of Probiotics in the Management of Chemotherapy-Induced Diarrhea: A Case Study]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/5/569?rss=1</link>
<description><![CDATA[
<p>Gastrointestinal disturbances (particularly diarrhea) are often induced in
response to cancer treatments such as chemotherapy or radiation. Oral
chemotherapeutic agents can induce diarrhea by damaging the intestinal lining.
Two common oral drugs used in cancer treatment that are known to have
gastrointestinal side effects are capecitabine and lapatinib. In this brief
communication, the authors discuss a case study of a stage IV breast cancer
patient whose chemotherapy-induced diarrhea was treated successfully with a
multispecies combination of probiotics. This is a unique study in which grade
3 chemotherapy-induced diarrhea (characterized by 7&ndash;9 stools per day and
associ ated with incontinence and abdominal cramping) was treated with only a
multispecies combination of probiotics. Probiotics have been used to treat
diarrhea in patients with irritable bowel syndrome, ulcerative colitis,
pouchitis, and Crohn's disease. More recently, probiotics have been used to
treat chemotherapy-induced diarrhea in colon cancer patients. This case study
demonstrates that the probiotics can also be used to treat severe cases of
chemotherapy-induced diarrhea in breast cancer patients. The use of different
probiotics in gastrointestinal diseases is an increasingly important area of
study, and more research into this area is needed. This study demonstrates
that probiotics should be considered for advanced breast cancer patients with
chemotherapy-induced diarrhea.</p>
]]></description>
<dc:creator><![CDATA[El-Atti, S. A., Wasicek, K., Mark, S., Hegazi, R.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109332004</dc:identifier>
<dc:title><![CDATA[Use of Probiotics in the Management of Chemotherapy-Induced Diarrhea: A Case Study]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>570</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>569</prism:startingPage>
<prism:section>Brief Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/5/571?rss=1">
<title><![CDATA[Effects of Intravenous Lipid Emulsions in Postoperative Patients]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/5/571?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Rollins, C. J.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109332775</dc:identifier>
<dc:title><![CDATA[Effects of Intravenous Lipid Emulsions in Postoperative Patients]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>572</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>571</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/5/573?rss=1">
<title><![CDATA[Use of Probiotics for Treatment of Chemotherapy-induced Diarrhea: Is It a Myth?]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/5/573?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Miller, A. C., Elamin, E. M.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109336596</dc:identifier>
<dc:title><![CDATA[Use of Probiotics for Treatment of Chemotherapy-induced Diarrhea: Is It a Myth?]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>574</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>573</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/5/575?rss=1">
<title><![CDATA[Letter to the Editor]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/5/575?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Thornton, S. N.]]></dc:creator>
<dc:date>Thu, 27 Aug 2009 13:41:07 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109333113</dc:identifier>
<dc:title><![CDATA[Letter to the Editor]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>575</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>575</prism:startingPage>
<prism:section>Letter to the Editor</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/4/358?rss=1">
<title><![CDATA["Do You Feel Misguided by All These Guidelines?"]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/4/358?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[McClave, S. A.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109339294</dc:identifier>
<dc:title><![CDATA["Do You Feel Misguided by All These Guidelines?"]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>360</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>358</prism:startingPage>
<prism:section>On My Mind: An Opportunity to Dialogue with A.S.P.E.N. President Steven A. McClave</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/361?rss=1">
<title><![CDATA[Defining and Classifying Cancer Cachexia: A Proposal by the SCRINIO Working Group]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/361?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Although cancer cachexia is widely diffuse in the
cancer patient population, there is no objective definition and classification
of this syndrome. The purpose of this study is to propose a simple and quick
classification that relies on the severity of the body weight loss and
presence/absence of symptoms that are associated with cancer cachexia.
<I>Methods:</I> The authors used a database of an ongoing multicenter
prospective investigation on the screening of the nutrition risk of 1307
cancer outpatients from different (mainly Italian) university or scientific
institutes or hospitals. The database included demographic, oncologic,
clinical, and nutrition data. The patients were divided into 4 classes based
on combinations of body weight loss (&lt;10%, precachexia; &ge;10%, cachexia)
and the presence/absence of at least 1 symptom of anorexia, fatigue, or early
satiation. The authors verified statistically whether these 4 classes were
associated with the distribution of main clinical, nutrition, and oncologic
variables, after adjustment for treatment status, by using the
Cochrane-Mantel-Hanszel test for count data and ANOVA for continuous data.
<I>Results:</I> Moving from "asymptomatic precachexia" (class 1)
to "symptomatic cachexia" (class 4), there were statistically
significant trends (<I>P</I> &lt; .0001) in the percentage of
gastrointestinal vs nongastrointestinal tumors, severity of cancer stage,
percentage of weight loss, number of symptoms per patient, Eastern Cooperative
Oncology Group (ECOG) performance status, and nutritional risk score.
<I>Conclusions:</I> The statistical analysis has validated the
classification by identifying stages with different severity of cachexia. This
classification could be adopted within a comprehensive oncologic approach to
the weight-losing patients, until more specific diagnostic techniques are
available in clinical practice.</p>
]]></description>
<dc:creator><![CDATA[Bozzetti, F., Mariani, L.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108325076</dc:identifier>
<dc:title><![CDATA[Defining and Classifying Cancer Cachexia: A Proposal by the SCRINIO Working Group]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>367</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>361</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/368?rss=1">
<title><![CDATA[Rationale and Design of the Pediatric Critical Illness Stress-Induced Immune Suppression (CRISIS) Prevention Trial]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/368?rss=1</link>
<description><![CDATA[
<p>Despite implementation of CDC recommendations and bundled interventions for
preventing catheter-associated blood stream infection, ventilator-associated
pneumonia, or urinary catheter&ndash;associated infections, nosocomial
infections and sepsis remain a significant cause of morbidity and mortality in
critically ill children. Recent studies suggest that acquired critical illness
stress-induced immune suppression (CRISIS) plays a role in the development of
nosocomial infection and sepsis. This condition can be related to inadequate
zinc, selenium, and glutamine levels, as well as hypoprolactinemia, leading to
stress-induced lymphopenia, a predominant T<SUB>H</SUB>2 monocyte/macrophage
state, and subsequent immune suppression. Prolonged immune dysfunction
increases the likelihood of nosocomial infections associated with invasive
devices. Although strategies to prevent common complications of critical
illness are routinely employed (eg, prophylaxis for gastrointestinal bleeding,
thrombophlebitis), no prophylactic strategy is used to prevent stress-induced
immune suppression. This is the authors' rationale for the pediatric CRISIS
prevention trial (NCT00395161), designed as a randomized, double-blind,
controlled clinical investigation to determine if daily enteral
supplementation with zinc, selenium, and glutamine as well as parenteral
metoclopramide (a dopamine 2 receptor antagonist that reverses
hypoprolactinemia) prolongs the time until onset of nosocomial infection or
sepsis in critically ill children compared to enteral supplementation with
whey protein. If effective, this combined nutritional and pharmacologic
approach may lessen the excess morbidity and mortality as well as resource
utilization associated with nosocomial infections and sepsis in this
population. The authors present the design and analytic plan for the CRISIS
prevention trial.</p>
]]></description>
<dc:creator><![CDATA[Carcillo, J., Holubkov, R., Dean, J. M., Berger, J., Meert, K. L., Anand, K. J. S., Zimmerman, J., Newth, C. J. L., Harrison, R., Willson, D. F., Nicholson, C., the Eunice Kennedy Shriver National Institute of Child Health and Human Development Collaborative Pediatric Critical Care Research Network]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108327392</dc:identifier>
<dc:title><![CDATA[Rationale and Design of the Pediatric Critical Illness Stress-Induced Immune Suppression (CRISIS) Prevention Trial]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>374</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>368</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/375?rss=1">
<title><![CDATA[Understanding Why Patients Die After Gastrostomy Tube Insertion: A Retrospective Analysis of Mortality]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/375?rss=1</link>
<description><![CDATA[
<p><I>Objectives:</I> To understand the causes of mortality of inpatients
receiving a percutaneous endoscopic gastrostomy (PEG) tube compared with a
survival curve predicted from a model proposed by Levine et al (2007).
<I>Design:</I> A retrospective study of patients receiving a PEG over an
18-month period. <I>Setting:</I> Royal United Hospital Bath, a district
general hospital in the southwest of England. <I>Patients:</I> Fifty-five
cases, with 44 found eligible for inclusion. <I>Interventions:</I> A Levine
score was calculated for this cohort. A survival curve after PEG was produced
and compared with the Kaplan-Meier curve predicted by the Levine model.
<I>Main Outcome Measures:</I> Mortality over a period of 1 year.
<I>Results:</I> The mortality at 1, 3, 6, and 12 months was 16%, 20%, 25%,
and 28%, respectively. This matched the predicted death rate from the Levine
model closely (Pearson's rank correlation coefficient = 0.96).
<I>Conclusions:</I> The authors found that the mortality of patients
receiving a PEG followed that predicted for a similar cohort of patients
without PEGs in the Levine model. This suggests that the deaths observed were
due to underlying comorbidities, can provide a baseline for mortality targets
for PEG services, and is useful patient information regarding the risks and
benefits of the procedure. The findings demonstrate that PEG does no harm and
supports the accepted opinion that nutrition support is associated with a
better outcome. Furthermore, they show that most deaths occur within the first
month of placement and would support arguments for delaying placement until
outcome from the underlying condition is more predictable.</p>
]]></description>
<dc:creator><![CDATA[Longcroft-Wheaton, G., Marden, P., Colleypriest, B., Gavin, D., Taylor, G., Farrant, M.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108327156</dc:identifier>
<dc:title><![CDATA[Understanding Why Patients Die After Gastrostomy Tube Insertion: A Retrospective Analysis of Mortality]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>379</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>375</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/380?rss=1">
<title><![CDATA[Nutrition Intervention: A Strategy Against Systemic Inflammatory Syndrome]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/380?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Sepsis and septic shock syndrome are the leading
causes of death in critically ill patients. Lipopolysaccharide (LPS) released
by the colonic microorganisms may translocate across a compromised lumen,
leading to upregulated reactive oxidative stress, inflammation, and sepsis.
The authors examined an enteral formula high in cysteine (antioxidant
precursor), -3 fatty acids, eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA), and prebiotic fructooligosaccharides (FOS) against
systemic inflammatory syndrome. <I>Methods:</I> Rats were allocated to (1)
standard soy-based diet high in cysteine and crude fiber and devoid of EPA-DHA
(CHOW); (2) whey-peptide-based liquid diet high in cysteine, EPA-DHA, and FOS
(CYSPUFA); or (3) casein-based liquid isonitrogenous diet, low in cysteine and
devoid of EPA-DHA-FOS (CASN). Liquid diets provided 25% and CHOW, 23% of
calories as protein. After 6 days on diets, rats received an intraperitoneal
injection of LPS or saline. Animals gained weight on their respective diets
and lost weight after LPS administration. The CYSPUFA group lost considerably
less weight (vs CASN or CHOW, <I>P</I> &lt; .05). Inflammatory cytokines
significantly increased by 4 hours and subsided 18 hours after assault. The
CASN group showed elevated liver enzyme alanine aminotransferase release from
damaged hepatocytes and developed severe hepatic pathology with low
hematocrit. The CHOW group developed more severe hepatic lesions compared with
those on liquid diets. Concentration of liver enzyme and pathology were
improved in rats receiving CYSPUFA. <I>Conclusions:</I> Data indicate that
CYSPUFA, a diet rich in EPA-DHA-FOS, protects against LPS-induced systemic
inflammatory responses and warrants clinical studies in critically ill
patients.</p>
]]></description>
<dc:creator><![CDATA[Oz, H. S., Chen, T. S., Neuman, M.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108327194</dc:identifier>
<dc:title><![CDATA[Nutrition Intervention: A Strategy Against Systemic Inflammatory Syndrome]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>389</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>380</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/390?rss=1">
<title><![CDATA[Effect of Dietary Fatty Acid Composition on Th1/Th2 Polarization in Lymphocytes]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/390?rss=1</link>
<description><![CDATA[
<p><I>Background</I>: It has become increasingly clear that polyunsaturated
fatty acids (PUFAs) have immunomodulatory effects. However, the intake of
these fatty acids used in animal studies often greatly exceeds dietary human
intake. Whether differences in the composition of fatty acids that are
consumed in amounts consistent with normal dietary intake can influence immune
function remains uncertain. <I>Methods</I>: We manufactured 3 types of
liquid diet, related to modified fatty acid composition (-6/-3 =
0.25, 2.27 and 42.9), but excluding eicosapentaenoic acid and docosahexaenoic
acid, based upon a liquid diet used clinically in humans. We assessed
CD3-stimulated cytokine production of splenocytes in female BALB/c mice (n = 4
per group) fed 1 of 3 liquid diets for 4 weeks. We also measured the cytokine
production of peripheral blood mononuclear cells stimulated with phorbol
myristate acetate and ionomycin in humans at the end of a 4-week period of
consumption of 2 different liquid diets (-6/-3 = 3 and 44).
<I>Results:</I> We found that the ratio of interfero -
(IFN-) / interleukin-4 (IL-4) was significantly higher in mice fed the
-3 rich diet than in others. In humans, IFN- / IL-4 was
significantly higher after the -3 versus the -6 enhanced diet.
<I>Conclusions</I>: Differences in the composition of -3 and
-6 PUFAs induces a shift in the Th1/Th2 balance in both mouse and human
lymphocytes, even when ingested in normal dietary amounts. An -3 rich
diet containing -linolenic acid modulates immune function.</p>
]]></description>
<dc:creator><![CDATA[Mizota, T., Fujita-Kambara, C., Matsuya, N., Hamasaki, S., Fukudome, T., Goto, H., Nakane, S., Kondo, T., Matsuo, H.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108325252</dc:identifier>
<dc:title><![CDATA[Effect of Dietary Fatty Acid Composition on Th1/Th2 Polarization in Lymphocytes]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>396</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>390</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/397?rss=1">
<title><![CDATA[Biofilms, Infection, and Parenteral Nutrition Therapy]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/397?rss=1</link>
<description><![CDATA[
<p>Parenteral nutrition therapy is used in patients with a contraindication to
the use of the gastrointestinal tract, and infection is one of its frequent
and severe complications. The objective of the present study was to detect the
presence of biofilms and microorganisms adhering to the central venous
catheters used for parenteral nutrition therapy by scanning electron
microscopy. Thirty-nine central venous catheters belonging to patients with
clinical signs of infection (G1) and asymptomatic patients (G2) and patients
receiving central venous catheters for clinical monitoring (G3) were analyzed
by semiquantitative culture and scanning electron microscopy. The central
venous catheters of G1 presented more positive cultures than those of G2 and
G3 (81% vs 50% and 0%, respectively). However, biofilms were observed in all
catheters used and 55% of them showed structures that suggested central venous
catheters colonization by microorganisms. Approximately 53% of the catheter
infections evolved with systemic infection confirmed by blood culture. The
authors conclude that the presence of a biofilm is frequent and is an
indicator of predisposition to infection, which may even occur in patients who
are still asymptomatic.</p>
]]></description>
<dc:creator><![CDATA[Machado, J. D. C., Suen, V. M. M., de Castro Figueiredo, J. F., Marchini, J. S.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108327526</dc:identifier>
<dc:title><![CDATA[Biofilms, Infection, and Parenteral Nutrition Therapy]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>403</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>397</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/404?rss=1">
<title><![CDATA[The Role of Pretreatment Percutaneous Endoscopic Gastrostomy in Facilitating Therapy of Head and Neck Cancer and Optimizing the Body Mass Index of the Obese Patient]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/404?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Chemoradiation of head and neck cancer induces severe
dysphagia and malnutrition, which may lead to interruptions in therapy and
reduction in its efficacy. Percutaneous endoscopic gastrostomy (PEG) feedings
bypass the oropharynx, allowing administration of nutrients and medications
into the stomach, thus preventing malnutrition, dehydration, and treatment
interruption. <I>Methods:</I> Medical records of 161 patients treated for
head and neck cancer who had PEGs placed prior to chemoradiation and 2 PEGs
placed during chemoradiation were reviewed from the date of PEG placement
throughout treatment and utilization. The objective was to determine the
contribution of pretreatment PEGs to the therapy of patients with head and
neck cancer and to optimize their body mass index. <I>Results:</I> Severe
chemoradiation-induced dysphagia developed in 160 patients (98%),
necessitating PEG utilization for feeding and hydration. PEGs were used for a
mean 251 &plusmn; 317 days. Significant complications related to PEG placement
and utilization were infrequent. PEG feeding allowed chemoradiation to
continue without interruption in 93% of patients. Individualized feeding
regimens optimized body mass index in obese and overweight patients with a
decline from 33.0 &plusmn; 3.4 to 28.4 &plusmn; 4.8 kg/m<sup>2</sup>
(<I>P</I> &lt; .001) and 27.3 &plusmn; 1.5 to 24.6 &plusmn; 2.7
kg/m<sup>2</sup> (<I>P</I> &lt; .001), respectively. Radiation-induced
strictures developed in 12% of patients, requiring endoscopic dilatation.
<I>Conclusions:</I> Enteral feeding through prechemoradiation-placed PEGs is
an effective and safe method for nutrition and hydration of patients with head
and neck cancer undergoing chemoradiation. PEGs allowed chemoradiation to
proceed with minimal interruptions despite severe dysphagia, which excluded
oral intake for prolonged periods.</p>
]]></description>
<dc:creator><![CDATA[Raykher, A., Correa, L., Russo, L., Brown, P., Lee, N., Pfister, D., Gerdes, H., Shah, J., Kraus, D., Schattner, M., Shike, M.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108327525</dc:identifier>
<dc:title><![CDATA[The Role of Pretreatment Percutaneous Endoscopic Gastrostomy in Facilitating Therapy of Head and Neck Cancer and Optimizing the Body Mass Index of the Obese Patient]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>410</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>404</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/411?rss=1">
<title><![CDATA[Starvation-Induced Proximal Gut Mucosal Atrophy Diminished With Aging]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/411?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Starvation induces small bowel atrophy with increased
intestinal epithelial apoptosis and decreased proliferation. The authors
examined these parameters after starvation in aged animals. <I>Methods:</I>
Sixty-four 6-week-old and 26-month-old C57BL/6 mice were randomly assigned to
either an ad libitum fed or fasted group. The small bowel was harvested at 12,
48, and 72 hours following starvation. Proximal gut mucosal height was
measured and epithelial cells counted. Apoptosis was identified by terminal
deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining.
Proliferation was determined by immunohistochemical staining for proliferating
cell nuclear antigen. Comparison of fed vs fasted and adult vs old groups was
done by one-way ANOVA with Tukey's test and unpaired Student's <I>t</I>
test. Significance was accepted at <I>P</I> &lt; .05. <I>Results:</I> Aged
mice had higher proximal gut weights, mucosal heights, and cell numbers at
baseline compared with the adult group (<I>P</I> &lt; .05). The rate of
apoptosis was lower in the aged (<I>P</I> &lt; .05), but proliferation was
not different between groups before starvation. After starvation, proximal gut
wet weight decreased only in adult mice (<I>P</I> &lt; .05). Gut mucosal
height and mucosal cell number decreased more in adult than in aged mice
(<I>P</I> &lt; .05). This was related to decreased proliferation only in the
adult group (<I>P</I> &lt; .05). The fold of epithelial apoptosis that
increased was higher in the aged group than in the adult group after
starvation (<I>P</I> &lt; .05). <I>Conclusions:</I> Gut mucosal kinetics
change with age and have lower rates of apoptosis and greater mucosal mass;
the character of starvation-induced atrophy is diminished with aging.</p>
]]></description>
<dc:creator><![CDATA[Song, J., Wolf, S. E., Wu, X.-W., Finnerty, C. C., Gauglitz, G. G., Herndon, D. N., Jeschke, M. G.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108325178</dc:identifier>
<dc:title><![CDATA[Starvation-Induced Proximal Gut Mucosal Atrophy Diminished With Aging]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>416</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>411</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/417?rss=1">
<title><![CDATA[Need for Thiamine in Peripheral Parenteral Nutrition After Abdominal Surgery in Children]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/417?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Thiamine blood concentrations of pediatric patients
receiving peripheral parenteral nutrition change during the postoperative
period. In addition, the need to administer thiamine after surgery has not yet
been fully studied in children receiving peripheral parenteral nutrition.
<I>Objective:</I> The objective of this prospective study is to clarify
whether pediatric patients require the administration of thiamine while
receiving peripheral parenteral nutrition after abdominal surgery.
<I>Patients:</I> Fifteen children were divided into 2 groups; 1 group
received peripheral parenteral nutrition without thiamine after surgery (n =
7), whereas the other group received peripheral parenteral nutrition with
thiamine after surgery (n = 8). In both groups, thiamine blood concentrations
were measured on the preoperative day, and changes in thiamine concentration
over time were measured during the starvation period from the first to the
fifth postoperative day. <I>Results:</I> Preoperative thiamine blood
concentrations were within the normal range in both groups. In the group
receiving peripheral parenteral nutrition without thiamine, the thiamine
concentration gradually decreased with time after the operation, whereas the
concentration remained within the normal range in the group receiving
peripheral parenteral nutrition with thiamine. Among the 7 patients receiving
peripheral parenteral nutrition without thiamine, the thiamine concentration
in 3 patients was below the normal range on the fifth postoperative day.
<I>Conclusion:</I> During the starvation period after abdominal surgery,
thiamine blood concentrations decreased in pediatric patients receiving
peripheral parenteral nutrition without thiamine. Therefore, clinicians
treating pediatric patients should add thiamine to the peripheral parenteral
nutrition solution during the short starvation period after abdominal
surgery.</p>
]]></description>
<dc:creator><![CDATA[Masumoto, K., Esumi, G., Teshiba, R., Nagata, K., Nakatsuji, T., Nishimoto, Y., Ieiri, S., Kinukawa, N., Taguchi, T.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108327391</dc:identifier>
<dc:title><![CDATA[Need for Thiamine in Peripheral Parenteral Nutrition After Abdominal Surgery in Children]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>422</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>417</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/423?rss=1">
<title><![CDATA[Effect of Sesame Oil on Acidified Ethanol-Induced Gastric Mucosal Injury in Rats]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/423?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Exposure of gastric mucosa to concentrated ethanol
induces acute gastritis. Gastric mucosal lipid peroxidation plays a
significant role in the pathogenesis of ethanol-induced gastric mucosal
lesions. The aim of this study was to investigate the effect of sesame oil on
acidified ethanol-induced gastric mucosal damage in rats. <I>Methods:</I> We
performed gastric bilateral vagotomy in rats. A small incision on forestomach
was made and stomach content was expelled. Normal artificial gastric acid (54
mM NaCl plus 100 mM HCl) or acidified ethanol (30% ethanol plus 150 mM HCl)
was instilled into the stomach. Gastric lipid peroxidation, glutathione, and
nitric oxide levels were measured 3 hours after acidified ethanol
administration. <I>Results:</I> Acidified ethanol caused mucosal ulceration,
luminal hemorrhage, lipid peroxidation, and a lower level of mucosal
glutathione and nitric oxide production. Pretreatment of sesame oil, but not
mineral oil, significantly decreased acidified ethanol-induced mucosal ulcer
formation and luminal hemorrhage. Sesame oil reduced mucosal lipid
peroxidation, as well as glutathione and nitric oxide production in acidified
ethanol-treated stomachs. Furthermore, both sesame oil and mineral oil did not
affect serum ethanol concentration in acidified ethanol-treated rats.
<I>Conclusion:</I> Sesame oil attenuates acidified ethanol-induced gastric
mucosal injury by reducing oxidative stress in rats.</p>
]]></description>
<dc:creator><![CDATA[Hsu, D.-Z., Chu, P.-Y., Liu, M.-Y.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108327046</dc:identifier>
<dc:title><![CDATA[Effect of Sesame Oil on Acidified Ethanol-Induced Gastric Mucosal Injury in Rats]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>427</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>423</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/428?rss=1">
<title><![CDATA[Ghrelin Does Not Predict Adaptive Hyperphagia in Patients With Short Bowel Syndrome]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/428?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Adaptive hyperphagia is associated with reduced
dependence on parenteral nutrition in patients with short bowel syndrome, but
mechanisms have not been described. Ghrelin (GHR) has orexigenic effects,
whereas peptide YY (PYY) reduces intake. GHR also acts as a hormone to control
body fat stores. The authors evaluated whether GHR or PYY was related to
caloric intake or absorption in patients with short bowel syndrome and whether
GHR was associated with body mass index. <I>Methods:</I> Patients were
admitted twice for nutrient balance. Height and body weight were obtained
using standardized protocols. Energy intake &gt;40 kcal/kg/day was defined as
adaptive hyperphagia. Fasting plasma PYY and GHR were assayed in duplicate
with Linco enzyme-linked immunosorbent assay kits. <I>Results:</I> The
median age of the 7 study participants was 62 (range, 45-66) years, time with
short bowel syndrome was 6.6 (range, 2-29) years, and body mass index was 21.2
kg/m<sup>2</sup> (range, 19-27.7). Five patients had adaptive hyperphagia.
Neither GHR nor PYY was significantly related to energy intake or absorption
(GHR: <I>R</I> = 0.22 and <I>R</I> = &ndash;0.233, PYY: <I>R</I> = 0.10
and <I>R</I> = &ndash;0.13). Body mass index trended toward an inverse
association with GHR (GHR: <I>R</I> = &ndash;0.540, <I>P</I> = .211).
<I>Conclusion:</I> The rigorous adaptive hyperphagia seen in these patients
with short bowel syndrome was not related to fasting GHR or PYY, suggesting
the need to explore other mechanisms.</p>
]]></description>
<dc:creator><![CDATA[Compher, C. W., Kinosian, B. P., Metz, D. C.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108324583</dc:identifier>
<dc:title><![CDATA[Ghrelin Does Not Predict Adaptive Hyperphagia in Patients With Short Bowel Syndrome]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>432</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>428</prism:startingPage>
<prism:section>Brief Communication</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/433?rss=1">
<title><![CDATA[Dexamethasone and GLP-2 Given to Lactating Rat Dams Influence Glucose Uptake in Suckling and Postweanling Offspring]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/433?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Glucagon-like peptide&ndash;2 (GLP-2) enhances
intestinal absorption in adult animals. Glucocorticosteroids accelerate the
ontogeny of the intestine and increase sugar uptake in adult animals.
Modifying the maternal diet during lactation alters nutrient uptake in the
offspring. The authors hypothesized that GLP-2 and dexamethasone, when
administrated to lactating rat dams, enhance sugar uptake in the suckling and
postweanling offspring. <I>Methods:</I> Rat dams were treated during
lactation with GLP-2 (0.1 &micro;g/g/day subcutaneously [SC], twice daily),
dexamethasone (0.128 &micro;g/g/day SC, once daily), GLP-2 + dexamethasone (same
doses), or placebo. The suckling offspring were sacrificed at 19&ndash;21 days
of age, and the postweanlings were sacrificed 4 weeks later. Intestinal
glucose and fructose uptake was assessed using an in vitro ring technique.
<I>Results:</I> GLP-2 and dexamethasone resulted in lower body weights, and
dexamethasone caused intestinal atrophy in sucklings. The jejunal atrophy in
sucklings given dexamethasone was prevented by GLP-2 + dexamethasone. In
sucklings, the maximal transport rate and the Michaelis affinity constant for
ileal glucose uptake were both increased by GLP-2 and GLP-2 + dexamethasone.
In contrast, in postweanlings, the maximal transport rate for jejunal glucose
uptake was reduced by dexamethasone and GLP-2, as was ileal fructose uptake.
<I>Conclusions:</I> Treating lactating rat dams with GLP-2 or dexamethasone
enhances glucose uptake in sucklings, but the late effect is a reduction in
glucose and fructose absorption in postweanlings. The nutritional significance
of these findings remains to be established.</p>
]]></description>
<dc:creator><![CDATA[Drozdowski, L., Iordache, C., Clandinin, M. T., Wild, G., Todd, Z., Thomson, A. B. R.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108324874</dc:identifier>
<dc:title><![CDATA[Dexamethasone and GLP-2 Given to Lactating Rat Dams Influence Glucose Uptake in Suckling and Postweanling Offspring]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>439</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>433</prism:startingPage>
<prism:section>Reviews</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/4/440?rss=1">
<title><![CDATA[Use of Nutrition to Prevent Stress-induced Immunosuppression in the Pediatric Intensive Care Unit: A Clinical Trials Minefield]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/4/440?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Neu, J.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108328521</dc:identifier>
<dc:title><![CDATA[Use of Nutrition to Prevent Stress-induced Immunosuppression in the Pediatric Intensive Care Unit: A Clinical Trials Minefield]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>441</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>440</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/4/442?rss=1">
<title><![CDATA[Do Obese Patients Have Specific Nutrition Goals in Cases of Cancer?]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/4/442?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Genton, L., Pichard, C.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108328655</dc:identifier>
<dc:title><![CDATA[Do Obese Patients Have Specific Nutrition Goals in Cases of Cancer?]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>443</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>442</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/4/444?rss=1">
<title><![CDATA[Comment On: Probiotic Prophylaxis in Predicted Severe Acute Pancreatitis: A Randomized, Double-Blind, Placebo-Controlled Trial]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/4/444?rss=1</link>
<description><![CDATA[
<p>BACKGROUND: Infectious complications and associated mortality are a major
concern in acute pancreatitis. Enteral administration of probiotics could
prevent infectious complications, but convincing evidence is scarce. Our aim
was to assess the effects of probiotic prophylaxis in patients with predicted
severe acute pancreatitis. METHODS: In this multicentre randomised,
double-blind, placebo-controlled trial, 298 patients with predicted severe
acute pancreatitis (Acute Physiology and Chronic health Evaluation [APACHE II]
score &gt; or =8, Imrie score &gt; or =3, or C-reactive protein &gt;150 mg/L)
were randomly assigned within 72 h of onset of symptoms to receive a
multispecies probiotic preparation (n = 153) or placebo (n = 145),
administered enterally twice daily for 28 days. The primary endpoint was the
composite of infectious complications&mdash;ie, infected pancreatic necrosis,
bacteraemia, pneumonia, urosepsis, or infected ascites&mdash;during admission
and 90-day follow-up. Analyses were by intention to treat. This study is
registered, number ISRCTN38327949. FINDINGS: One person in each group was
excluded from analyses because of incorrect diagnoses of pancreatitis; thus,
152 individuals in the probiotics group and 144 in the placebo group were
analysed. Groups were much the same at baseline in terms of patients'
characteristics and disease severity. Infectious complications occurred in 46
(30%) patients in the probiotics group and 41 (28%) of those in the placebo
group (relative risk 1.06, 95% CI 0.75-1.51). 24 (16%) patients in the
probiotics group died, compared with nine (6%) in the placebo group (relative
risk 2.53, 95% CI 1.22-5.25). Nine patients in the probiotics group developed
bowel ischaemia (eight with fatal outcome), compared with none in the placebo
group (p = 0.004). INTERPRETATION: In patients with predicted severe acute
pancreatitis, probiotic prophylaxis with this combination of probiotic strains
did not reduce the risk of infectious complications and was associated with an
increased risk of mortality. Probiotic prophylaxis should therefore not be
administered in this category of patients. (<I>Lancet</I>.
2008;371:651-659)</p>
<p><b>Besselink MG, van Santvoort HC, Buskens E, et al; Dutch Acute
Pancreatitis Study Group</b></p>
]]></description>
<dc:creator><![CDATA[McClave, S. A., Heyland, D. K., Wischmeyer, P. E.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108331176</dc:identifier>
<dc:title><![CDATA[Comment On: Probiotic Prophylaxis in Predicted Severe Acute Pancreatitis: A Randomized, Double-Blind, Placebo-Controlled Trial]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>446</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>444</prism:startingPage>
<prism:section>eJournal</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/4/447?rss=1">
<title><![CDATA[Letter to the Editor]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/4/447?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Hemila, H.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108328520</dc:identifier>
<dc:title><![CDATA[Letter to the Editor]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>448</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>447</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/4/449?rss=1">
<title><![CDATA[Author Response]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/4/449?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Cotton, B. A., Dossett, L. A., Collier, B. R.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108328654</dc:identifier>
<dc:title><![CDATA[Author Response]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>449</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>449</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/4/450?rss=1">
<title><![CDATA[Letter to the Editor]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/4/450?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Wanten, G. J.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108328469</dc:identifier>
<dc:title><![CDATA[Letter to the Editor]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>450</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>450</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/4/451?rss=1">
<title><![CDATA[Letter to the Editor]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/4/451?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Driscoll, D. F.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108328471</dc:identifier>
<dc:title><![CDATA[Letter to the Editor]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>452</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>451</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/4/453?rss=1">
<title><![CDATA[Letter to the Editor]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/4/453?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Correia, M. I. T. D.]]></dc:creator>
<dc:date>Thu, 11 Jun 2009 09:13:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108329705</dc:identifier>
<dc:title><![CDATA[Letter to the Editor]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>454</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>453</prism:startingPage>
<prism:section>Letters to the Editor</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/3/255?rss=1">
<title><![CDATA[Clinical Guidelines for the Use of Parenteral and Enteral Nutrition in Adult and Pediatric Patients, 2009]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/3/255?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) Board of Directors]]></dc:creator>
<dc:date>Mon, 27 Apr 2009 11:13:19 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109333115</dc:identifier>
<dc:title><![CDATA[Clinical Guidelines for the Use of Parenteral and Enteral Nutrition in Adult and Pediatric Patients, 2009]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>259</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>255</prism:startingPage>
<prism:section>Clinical Guidelines</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/3/260?rss=1">
<title><![CDATA[A.S.P.E.N. Clinical Guidelines: Nutrition Support of the Critically Ill Child]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/3/260?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mehta, N. M., Compher, C., A.S.P.E.N. Board of Directors]]></dc:creator>
<dc:date>Mon, 27 Apr 2009 11:13:19 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109333114</dc:identifier>
<dc:title><![CDATA[A.S.P.E.N. Clinical Guidelines: Nutrition Support of the Critically Ill Child]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>276</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>260</prism:startingPage>
<prism:section>Clinical Guidelines</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/reprint/33/3/277?rss=1">
<title><![CDATA[Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient:: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.)]]></title>
<link>http://pen.sagepub.com/cgi/reprint/33/3/277?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[McClave, S. A., Martindale, R. G., Vanek, V. W., McCarthy, M., Roberts, P., Taylor, B., Ochoa, J. B., Napolitano, L., Cresci, G., the A.S.P.E.N. Board of Directors, the American College of Critical Care Medicine]]></dc:creator>
<dc:date>Mon, 27 Apr 2009 11:13:19 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607109335234</dc:identifier>
<dc:title><![CDATA[Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient:: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.)]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>316</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>277</prism:startingPage>
<prism:section>Clinical Guidelines</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/3/317?rss=1">
<title><![CDATA[An Evaluation of the Neuroendocrine Response to Sleep in Pediatric Burn Patients]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/3/317?rss=1</link>
<description><![CDATA[
<p><I>Introduction:</I> Previous work demonstrated reduced stage 3+4 and
rapid eye movement (REM) sleep following burn injury. This study evaluated the
hormonal effects of drug intervention on measures of endocrine status. A
secondary objective examined the relationship between hormones and sleep stage
distribution. <I>Methods:</I> Forty patients 3&ndash;18 years of age with a
mean percent total body surface area burn of 50.1 &plusmn; 2.9 were randomly
assigned to zolpidem or haloperidol utilizing a blinded crossover design.
Polysomnography was performed 6 nights, 3/week over 2 weeks. Each week's first
night of monitoring was conducted without medication, serving as a baseline.
Hormonal levels (epinephrine, norepinephrine, growth hormone, melatonin,
dehydroepiandrosterone [DHEA], serotonin, cortisol) were obtained at 0600 h
each study day. <I>Results:</I> Both drugs were associated with increased
DHEA levels (<I>P</I> &lt; .03); no other hormones were affected by
medication. Significant inverse correlation was observed between REM sleep and
epinephrine (<I>r</I> = &ndash;.34, <I>P</I> = .004) and norepinephrine
levels (<I>r</I> = &ndash;.45, <I>P</I> = .02). A positive relationship
existed between serotonin and sleep stage 3+4 (<I>r</I> = 0.24, <I>P</I> =
.01) and REM (<I>r</I> = 0.48, <I>P</I> = .01). No other significant
associations were identified between hormones and sleep. <I>Conclusions:</I>
This work characterizes the relationship between sleep deprivation and select
endocrine parameters postburn. Drug interventions utilized in this study were
either ineffective or insufficient in modulating improved hormonal response.
Significance of zolpidem's and haloperidol's effect on serum levels of DHEA is
unclear. The inverse correlation of epinephrine with REM may suggest that
hypermetabolism associated with burns is partly due to lack of REM sleep.
Questions remain regarding the effects of sleep deprivation on metabolism and
clinical outcome.</p>
]]></description>
<dc:creator><![CDATA[Gottschlich, M. M., Khoury, J., Warden, G. D., Kagan, R. J.]]></dc:creator>
<dc:date>Mon, 27 Apr 2009 11:13:19 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108325180</dc:identifier>
<dc:title><![CDATA[An Evaluation of the Neuroendocrine Response to Sleep in Pediatric Burn Patients]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>326</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>317</prism:startingPage>
<prism:section>Reviews</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/3/327?rss=1">
<title><![CDATA[Hepatic Indicators of Oxidative Stress and Tissue Damage Accompanied by Systemic Inflammation in Rats Following a 24-Hour Infusion of an Unstable Lipid Emulsion Admixture]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/3/327?rss=1</link>
<description><![CDATA[
<p><I>Background:</I> Use of lipid emulsions in parenteral nutrition therapy
is an important source of daily energy in substitution of potentially harmful
glucose calories when given in excess in the intensive care unit. When added
to parenteral nutrition (PN) admixtures as a total nutrient admixture (TNA),
the stability and safety of the emulsion may be compromised. Development of a
rat model of a stable vs unstable lipid infusion would enable a study of the
potential risk. <I>Design:</I> Prospective, randomized, controlled study.
<I>Methods:</I> Surgical placement of a jugular venous catheter for the
administration of TNAs was performed. Two groups were studied: a stable or
s-TNA (n = 16) and an unstable or u-TNA (n = 17) as a 24-hour continuous
infusion. Stability of TNAs was determined immediately before and after
infusion using a laser-based method approved by the United States
Pharmacopeia. <I>Results:</I> Blood levels of aspartate aminotransferase,
glutathione-S-transferase, and C-reactive protein were significantly elevated
in u-TNA vs s-TNA (<I>P</I> &lt; .05). Also, liver tissue concentrations of
malondialdehyde were significantly higher in the u-TNA group (<I>P</I> &lt;
.05), and triglyceride tissue levels were also higher in u-TNA and approached
statistical significance (<I>P</I> = .077). <I>Conclusions:</I> Unstable
lipid infusions over 24 hours produce evidence of hepatic accumulation of fat
associated with oxidative stress, liver injury, and a low-level systemic
inflammatory response.</p>
]]></description>
<dc:creator><![CDATA[Driscoll, D. F., Ling, P.-R., Andersson, C., Bistrian, B. R.]]></dc:creator>
<dc:date>Mon, 27 Apr 2009 11:13:19 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108327155</dc:identifier>
<dc:title><![CDATA[Hepatic Indicators of Oxidative Stress and Tissue Damage Accompanied by Systemic Inflammation in Rats Following a 24-Hour Infusion of an Unstable Lipid Emulsion Admixture]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>335</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>327</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

<item rdf:about="http://pen.sagepub.com/cgi/content/abstract/33/3/336?rss=1">
<title><![CDATA[Cumulative Energy Imbalance in the Pediatric Intensive Care Unit: Role of Targeted Indirect Calorimetry]]></title>
<link>http://pen.sagepub.com/cgi/content/abstract/33/3/336?rss=1</link>
<description><![CDATA[
<p><I>Introduction:</I> Failure to accurately estimate energy requirements
may result in underfeeding or overfeeding. In this study, a dedicated
multidisciplinary nutrition team measured energy expenditure in critically ill
children. <I>Methods:</I> Steady-state indirect calorimetry was used to
obtain measured resting energy expenditure, which was compared with
equation-estimated energy expenditure and the total energy intake for each
subject. The children's metabolic status was examined in relation to standard
clinical characteristics. <I>Results:</I> Sixteen measurements were
performed in 14 patients admitted to the multidisciplinary pediatric intensive
care unit over a period of 12 months. Mean age of subjects in this cohort was
11.2 years (range 1.6 months to 32 years) and included 7 males and 7
postoperative patients. Altered metabolism was detected in 13 of 14 subjects
and in 15 of 16 (94%) measurements. There was no correlation between the
metabolic status of subjects and their clinical characteristics. Average daily
energy balance was 200 kcal/d (range &ndash;518 to +859 kcal/d). Agreement
between measured resting energy expenditure and equation-estimated energy
expenditure was poor, with mean bias of 72.3 &plusmn; 446 kcal/d (limits of
agreement &ndash;801.9 to + 946.5 kcal/d). <I>Conclusions:</I> A disparity
was observed between equation-estimated energy expenditure, measured resting
energy expenditure, and total energy intake, with a high incidence of
underfeeding or overfeeding. A wide range of metabolic alterations were
recorded, which could not be accurately predicted using standard clinical
characteristics. Targeted indirect calorimetry on high-risk patients selected
by a dedicated nutrition team may prevent cumulative excesses and deficits in
energy balance.</p>
]]></description>
<dc:creator><![CDATA[Mehta, N. M., Bechard, L. J., Leavitt, K., Duggan, C.]]></dc:creator>
<dc:date>Mon, 27 Apr 2009 11:13:19 PDT</dc:date>
<dc:identifier>info:doi/10.1177/0148607108325249</dc:identifier>
<dc:title><![CDATA[Cumulative Energy Imbalance in the Pediatric Intensive Care Unit: Role of Targeted Indirect Calorimetry]]></dc:title>
<dc:publisher>The American Society for Parenteral &amp; Enteral Nutrition</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>33</prism:volume>
<prism:endingPage>344</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>336</prism:startingPage>
<prism:section>Original Communications</prism:section>
</item>

</rdf:RDF>